Ivor Cummins and the Cholesterol Conundrum

In my quest to learn more about cholesterol especially given my history of developing paradoxically elevated LDL-C, LDL-P, Small LDL-P and Total cholesterol after eating low carb (here are my most recent blood lipids), I’ve scoured the net wide and far, even venturing deep into strange forums and comment threads… and still haven’t come across any clear answers.

Why does 1/3 of the population who eat low carb develop the sky rocketing levels of cholesterol when the remaining 2/3 demonstrate no change or a dramatic decrease?

In my journeys to the corners of the net to learn more, a few folks directed me to the work of Ivor Cummins, a chemical engineer who developed a deep interest in all things cholesterol (you can read more of his stuff at thefatemperor.com).

They recommended this lecture in particular:

I’ve finally gotten around to taking the time to watch through all 1 hr and 47 minutes of it and took some notes which I will share with you all below.

He does a wonderful job of covering cholesterol metabolism and biochemistry as well as addressing why dietary cholesterol and fat aren’t the problems they’ve been made out to be, when the real culprit is dietary carbohydrate. All material people who follow my stuff regularly will be familiar with and can be found in Jimmy Moore’s very readable Cholesterol Clarity.

While Ivor does a better job than Jimmy about going into the source research material, he does have a pretty thick Irish accent which I found made the lecture that much more interesting. The BJJ Cavewife however, who has trouble with accents, couldn’t understand a word!

I got excited at one point when Ivor began addressing the changes in blood lipids seen with a low carbohydrate diet and how dramatic the improvements can be… but was a bit let down because he never addresses the main question that I have, which is why do some folks who eat low carb paradoxically develop high cholesterol…. so I’ll have to continue on with my search!

Notes from this lecture

Key molecules

Cholesterol fundamental to life. Cells need it. Hormones need it.

Important in damage repair system.

Cholesterol blamed for disease like blaming paramedics at the scene of an accident.

Triglycerides – comes from diet. Can also be synthesized by body.

Key particles

Lipoprotein particles. These are needed to transport cholesterol and triglycerides because they are hydrophobic. Lipoproteins packages these cholesterols and triglycerides so they can be transported throughout the body, the outer shell is hydrophilic.

Lipoprotein particles are like boats, and the triglycerides and cholesterol are the cargo.

VLDL: contains 2:1 trigs to cholesterol. Made in the liver. As it moves through the body, and gets smaller as it unloads is cargo, and becomes LDL. Has a B100 surface protein marker.

sdLDL: small dense LDL. This is the bad one. If you have lots of these, it’s indicative of a dysfunctional system. Oxidized LDL also tracks this measurement. Oxidized LDL are the damaged versions and no longer work as they are supposed to.

HDL: Does a lot of good work.

Athersclerosis:

When a sLDL ends up in the vessel wall, your body recognizes this as a problem, and a defensive cell, the macrophage, goes after it and eats it, and becomes a blobby ‘foam’ cell. It looks foamy under the microscope because it gets filled up with all the fatty material.

And this builds up in the artery wall, building a plaque, and clogging the system.

How the cholesterol processing system works:

Chylomicron – created in gut when consuming dietary fat. It takes the cholesterol and triglycerides, mostly triglycerides, and is packaged into chylomicrons, and this goes into the blood stream.

It goes into they system and docks with muscle cells and fat cells and deposits it into those cells.

As it gives off its cargo, it shrinks, and becomes a chylomicron remnant, and only survive for around 20 minutes.. These go back to the liver, where they’re recycled.

I, too, have seen my cholesterol numbers go up since I (mostly) removed carbohydrates from my diet in July of 2011. I read Why We Get Fat in March of 2011 and was inspired to change my diet. I gradually reduced my sugar/carb consumption until deciding to go as close to zero as I could while retaining vegetables, peanuts and 90% chocolate in my diet. I have consumed between 10g & 30g (net) carbs on a daily basis for over four years now. (I do not take days off.) I do consume coffee & alcohol daily as well.

I am somewhat ambivalent about these numbers, tending more towards not so concerned. Mainly because my HDL is very high and my triglycerides remain relatively low; my TG/HDL ratio has been <1 for at least a couple years. My C-Reactive is also low. Also, I have never had my LDL or LDL particles directly measured.

Observations of Interest:
• The November 2011 re-test of the October 2011 lipid panel was ordered by my physician due to concern over the October numbers. He asked me what I had done between the tests to lower my cholesterol. Nothing, of course. Which makes me suspicious of the accuracy of any of these numbers.

• Before giving up sugar I consumed massive quantities of it (multiple daily sodas, ice cream after dinner and before bed…). I am 6' and never weighed more than 165 lbs. Lucky metabolism. My glucose level has INCREASED on my very low carb diet.

• It was not until the 2014/11 blood work that ketones ("Trace") showed up. I may consume to much protein to regularly be in ketosis.

I am looking forward to reading all the links in your post and starting up again own investigation into why my lipid levels have gone where they have.

I mean I don’t think I’ve seen an increase in fasting blood sugars before in someone who is low carb. Your trigs confirm that you’re predominantly low carb, but your blood glucose is higher than expected, as is your hbA1c.

I’m not sure how to put it altogether except to say that maybe the glucose numbers are spurious? Maybe you were stressed or something when you had the blood test, leading to increased cortisol and stress hormones, causing increased glucose in the blood…

It may be instructive to get a blood glucose monitor at home to see where you are over the course of a week or a month.

In any case, looks like we’re on the same path right now. Welcome to the journey into the unknown!

“In the Framingham Offspring Study, isolated HDL levels lower than the median are associated with a low risk of CHD. These data suggest that isolated low HDL may not be an atherogenic phenotype, Dr. Michael Miller said at the annual meeting of the American College of Cardiology.

While it’s well established that low HDL is associated with increased CHD risk, the risk in patients with isolated low HDL hasn’t been well studied. Yet low HDL together with an LDL below 100 mg/dL and a triglyceride level below 100 mg/dL is not a rare combination. It represented 7.4% of all study participants with low HDL, as defined by a level below the median, meaning less than 42 mg/dL in men and 54 mg/dL in women, noted Dr. Miller, professor of medicine, epidemiology, and preventive medicine and director of the center for preventive cardiology at the University of Maryland, Baltimore.

He reported on 3,560 adults in the Framingham Offspring Study with baseline lipid measurements recorded in 1987-1991. During a mean follow-up of 18 years, the incidence of newly diagnosed CHD was low in participants with isolated low HDL: just 5%. That was similar to the 4% incidence in subjects with above average HDL and low LDL and triglycerides. In contrast, when low HDL was present in subjects with higher LDL and/or triglycerides, the incidence of CHD was higher. So was the relative risk of CHD in a multivariate analysis after adjustment for age, sex, smoking status, diabetes, and hypertension.

When low HDL was present in combination with an LDL greater than 130 mg/dL along with triglycerides elevated above cut points of 150 and 200 mg/dL, the incident CHD rates climbed to 20%-25%, with adjusted hazard ratios of 1.7-2, compared with the risk in subjects with isolated low HDL.

What if the higher levels aren’t really an issue?
Suppose : if your nitric oxide levels are sufficient to keep endothelium from hardening and forming lesions wouldn’t the cholesterol levels cease to be an issue?

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